Abstract
Helicobacter pylori, a bacterial pathogen that can infect human stomach causing gastritis, ulcers and cancer, is known to have a high degree of genome/epigenome diversity as the result of mutation and recombination. The bacteria often infect in childhood and persist for the life of the host. One of the reasons of the rapid evolution of H. pylori is that it changes its genome drastically for adaptation to a new host. To investigate microevolution and adaptation of the H. pylori genome, we undertook whole genome sequencing of the same or very similar sequence type in multi-locus sequence typing (MLST) with seven genes in members of the same family consisting of parents and children in Japan. Detection of nucleotide substitutions revealed likely transmission pathways involving children. Nonsynonymous (amino acid changing) mutations were found in virulence-related genes (cag genes, vacA, hcpDX, tnfα, ggt, htrA and the collagenase gene), outer membrane protein (OMP) genes and other cell surface-related protein genes, signal transduction genes and restriction-modification genes. We reconstructed various pathways by which H. pylori can adapt to a new human host, and our results raised the possibility that the mutational changes in virulence-related genes have a role in adaptation to a child host. Changes in restriction-modification genes might remodel the methylome and transcriptome to help adaptation. This study has provided insights into H. pylori transmission and virulence and has implications for basic research as well as clinical practice.
Highlights
The pathogenic epsilon-proteobacterium Helicobacter pylori is a major cause of human gastric diseases [1]
Families infected with H. pylori of the same or very similar multi-locus sequence typing (MLST) sequence type
The allele type numbers of some of the seven MLST genes were different in families K-3 and K-4; this is based on a single nucleotide substitution, so we regard them as very similar sequences
Summary
The pathogenic epsilon-proteobacterium Helicobacter pylori is a major cause of human gastric diseases [1]. The H. pylori genome sequence exhibits a high degree of diversity even between closely related strains because of the high rate of mutation and recombination [2,3,4,5,6]. Microevolution in Helicobacter pylori Familial Infection grants for Scientific Research 20132033 to S.K.) from JSPS; the global COE project of Genome Information Big Bang from MEXT to I.K.; Grant in Promotion of Basic Research Activities for Innovative Biosciences 121205003001002100019) from Bio-oriented Technology Research Advance Institution to I.K.; Cooperative Research Grant of the Genome Research for BioResource, NODAI Genome Research Center, Tokyo University of Agriculture; and from the Takeda Science Foundation to Y.F
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